The anti-tumor effects of calorie restriction are correlated with reduced oxidative stress in ENU-induced gliomas.

作者: Megan A. Mahlke , Lisa A. Cortez , Melanie A. Ortiz , Marisela Rodriguez , Koji Uchida

DOI: 10.3402/PBA.V1I0.7189

关键词: Internal medicineApoptosisProtein oxidationEndocrinologyCalorie restrictionPathologyLipid peroxidationBiologyNitrotyrosineOxidative stressGliomaMalondialdehyde

摘要: The anti-tumor effects of calorie restriction (CR) and the possible underlying mechanisms were investigated using ethylnitrosourea (ENU)-induced glioma in rats. ENU was given transplacentally at gestational day 15, male offspring used this experiment. brain from 4-, 6-, 8-month-old rats fed either ad libitum (AL) or calorie-restricted diets (40% total calories compared to AL rats) studied. Tumor burden assessed by comparing number size gliomas present sections brain. Immunohistochemical analysis document lipid peroxidation [4-hydroxy-2-nonenal (HNE) malondialdehyde (MDA)], protein oxidation (nitrotyrosine), glycation AGE formation [methylglyoxal (MG) carboxymethyllysine (CML)], cell proliferation activity [proliferating nuclear antigen (PCNA)], death [single-stranded DNA (ssDNA)], presence thioredoxin 1 (Trx1), heme oxygenase-1 (HO-1) associated with development gliomas. results showed that did not change age groups; however, average significantly larger group younger groups. Immunopositivity observed mainly tumor cells reactive astrocytes all histological types ENU-induced glioma. Immunopositive areas for HNE, MDA, nitrotyrosine, MG, CML, HO-1, Trx1 increased growth CR both reduced gliomas, tumors exhibited less accumulation oxidative damage, decreased glycated end products, a HO-1 group. Furthermore, PCNA positive more ssDNA cells, which are correlated retarded tumors. Interestingly, we also discovered hypoxiainducible factor-1α (HIF-1α) levels normal tissue. Our very exciting because they only demonstrate but indicate mechanisms, i.e. investigation Trx1, apoptosis, HIF-1α. Keywords: restriction; ethylnitrosourea; glioma; stress; HIF-1α (Published: June 2011) Citation: Pathobiology Aging & Age-related Diseases 2011, : 7189 - DOI: 10.3402/pba.v1i0.7189

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